Search Results (4)

Background/Objectives: Enteric glial cells (EGCs) are non-neuronal cells of the enteric nervous system that contribute to intestinal homeostasis through interactions with the intestinal epithelium, enteric neurons, and resident intestinal immune cells. The objective of the current study was to determine how exposure of EGCs to short-chain fatty acids (SCFAs) would affect the expression of growth factors and pro-inflammatory cytokines, products of EGCs with known effects on intestinal epithelial barrier integrity. Methods: An enteroglial cell line was treated with low- (1 mM) or high- (10 mM) dose sodium butyrate or sodium propionate for 8 to 24 h, after which mRNA and protein levels of glial cell line-derived neurotrophic factor (GDNF), transforming growth factor β-1 (TGFβ-1), tumor necrosis factor α (TNFα), interleukin-6 (IL-6), and interleukin-1β (IL-1β) were measured using quantitative polymerase chain reaction assays and Western immunoblotting. Results: Only butyrate treatment for 8 and 24 h was associated with modest changes in GDNF mRNA. Neither SCFA elicited changes in TGFβ-1 mRNA. Despite this, high-dose butyrate and propionate were associated with reduced basal levels of TGFβ-1 protein as early as 12 h after treatment. Only butyrate was associated with a significant reduction in basal TNFα expression, which was present up to 24 h post-treatment. However, both butyrate (low- and high-dose) and propionate (high-dose only) elicited marked increases in IL-6 expression at all time points examined. Changes in cytokine mRNA levels were not mirrored at the protein level. Conclusions: SCFAs directly influence growth factor and cytokine expression in EGCs, but the functional implications of these changes in expression within the complicated milieux of the intestinal environment remain to be explored. Full article

Background: Gastrointestinal (GI) disturbances occur frequently in the early premotor stage of Parkinson’s disease (PD). These GI impairments are associated, at least in part, with dopaminergic dysfunction in the myenteric plexus. However, the enteric nervous system (ENS) pathophysiology underlying GI dysfunction in PD has been overlooked. Objectives: The aim of this study was to evaluate the premotor GI disturbances in rats submitted to intranasal (i.n.) MPTP, a valid experimental model of the premotor stage of PD. Methods: Ileum segments from male Wistar rats (21 weeks old) were collected 12 days following the i.n. MPTP administration for functional studies. Isometric contractile concentration–response (CR) curves (cumulative) for dopamine (DA) were performed in both the presence and absence of sulpiride, a selective dopamine D2-like receptor (D2R) antagonist. Results: Functional studies showed that DA induced a concentration-dependent contractile response in the ileum, which exhibited marked contraction at lower concentrations (0.01–0.9 µM) and relaxation at higher concentrations (3–90 µM). MPTP significantly attenuated both the contraction and the ensuing relaxation. Furthermore, sulpiride significantly reduced the contractile response to DA in the control group and blocked the relaxation in the MPTP group. The MPTP-induced dysmotility occurred with preserved DA homeostasis, as shown by normal DA, TH, and D2R ileal levels in the MPTP group. However, MPTP seemed to impose a decrease in S100β and GFAP (enteroglial markers) immunostaining in the ileal myenteric plexus. Conclusions: In summary, we provide pioneering functional, neurochemical, and morphological evidence showing that rats submitted to the i.n. MPTP model exhibited premotor DA-dependent ileum motile dysfunction accompanied by enteroglial disturbance within the myenteric plexus, but with preserved DA markers. Full article

The calcium-binding S100B protein is concentrated in glial cells (including enteroglial cells) in the nervous system. Its conformation and amino acid composition are significantly conserved in different species; this characteristic suggests conserved biological role(s) for the protein. The biological activity is concentration-dependent: low physiological concentrations exert a neurotrophic effect, while high concentrations exert a proinflammatory/toxic role. The proinflammatory/toxic role of S100B currently attracts the scientific community’s primary attention, while the protein’s physiological action remains unraveled—yet remarkably interesting. This is now a topical issue due to the recently consolidated notion that S100B is a natural trophic nutrient available in breast milk and/or other aliments, possibly interacting with other body districts through its impact on microbiota. These recent data may offer novel clues to understanding the role of this challenging protein. Full article

This in vivo study in mice addresses the relationship between the biodiversity of the microbiota and the levels of S100B, a protein present in enteroglial cells, but also in foods such as milk. A positive significant correlation was observed between S100B levels and Shannon values, which was reduced after treatment with Pentamidine, an inhibitor of S100B function, indicating that the correlation was influenced by the modulation of S100B activity. Using the bootstrap average method based on the distribution of the S100B concentration, three groups were identified, exhibiting a significant difference between the microbial profiles. Operational taxonomic units, when analyzed by SIMPER analysis, showed that genera regarded to be eubiotic were mainly concentrated in the intermediate group, while genera potentially harboring pathobionts often appeared to be more concentrated in groups where the S100B amounts were very low or high. Finally, in a pilot experiment, S100B was administered orally, and the microbial profiles appeared to be modified accordingly. These data may open novel perspectives involving the possibility of S100B-mediated regulation in the intestinal microbiota. Full article